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• W2609105514 abstract "Inflammatory diseases with unknown aetiology constantly undergo re-evaluation of their pathophysiology. Presently defining the human microbiome presents as a fascinating new era in medicine. As a consequence, old concepts such as the role of hidden bacterial foci causing disease undergo revival. This has been a principal concept until the twenties of the last century. Before that time and even later, legions of patients had to undergo removal of their tonsillae, their teeth were pulled out, and infected tissues at other sites underwent surgical clearing. It was thought that persisting bacterial foci were responsible for disease. The paper by Ungprassert and co-workers in this issue of JEADV1 critically examines existing evidence whether two distinct inflammatory disorders, periodontitis and psoriasis, are correlated. Periodontitis is a chronic inflammatory disorder of the periodontium, which consists of the gingiva, the periodontal ligament and the alveolar bone. In its severe form, it affects nearly a third or more of adults in the USA, and if untreated, it may cause loss of teeth. Porphyromonas gingivalis (P. gingivalis) acts as principal anaerobic agent with further bacteria participating (Treponema denticola, Tannerella forsythia). Disturbances of this polymicrobial synergy result in dysbiosis and disease. Thus, polymicrobial dysbiosis is now considered to be responsible for destructive inflammation of the periodontal site. In rheumatological disorders, for example rheumatoid arthritis, it has been shown that periodontitis is responsible for increased risk of systemic inflammatory disorders. In fact, periodontitis correlates with increased risk of rheumatoid arthritis, atherosclerosis and lung disease.2 The meta-analysis by Ungprassert et al.1 provides a careful analysis of published cohort as well as case–control studies and concentrates on the question whether periodontitis is associated with an increased risk of psoriasis. On the basis of critically examined papers, the authors found that persons with periodontitis show a significantly (1.55-fold) increased risk of psoriasis. These results further extend the list of associated disorders (comorbidities) seen in psoriasis patients. Also such data now should produce happy feelings in elderly dermatologist who lived through lifelong uncertainties of not knowing whether rotten teeth affect psoriasis. The question remains what mechanism(s) are responsible in creating this correlating set of disorders. As pointed out by the authors, immune activation by dysbiotic pathogens is likely to play a role. Clearly, a conversion of symbiotic microbiota to dysbiotic ones in susceptible carriers appears as a first step in periodontitis. In this situation, P. gingivalis remains key pathogen which is known to be able to activate innate (including complement with generation of C5a) as well as adaptive immune responses. Also the inflammatory response in gingival sites is almost purely neutrophilic. In psoriasis, early lesions as well as short-lived inflammatory burst (Pinkus’ squirting papilla, hot spots) are neutrophilic.3 In affected gingival sites as well as in psoriatic str. corneum, high amounts of the C5a were found.4 The complement split product C5a is one of the most potent chemotaxin for neutrophils. This points towards innate (P. gingivalis)-induced immune activation. From animal work and by epidemiological studies, it was suggested that oral pathogens may disturb systemic immune balance.5 Also P. gingivalis has been demonstrated to be able to evade into circulation from gingival sites eliciting systemic inflammation. In cardiovascular disease, these gingival pathogens have been noted to be located within atherosclerotic plaques.6 So far no evidence for gingival pathogens including P. gingivalis has been seen in psoriasis. The results produced by the meta-analysis of Ungprasert and co-workers demonstrate an association of periodontitis with psoriasis. Conceptually, dysbiotic oral bacteria may act as immune potentiators in susceptible persons. Many questions are now and again waiting to be answered including lifestyle, role of susceptibility genes and phenotype characterization of psoriasis patients. Dermatologists may now extend their search for comorbidities by looking into oral cavities as well. Still the mechanisms regulating focal gingival inflammation and psoriatic lesional activity remain unsolved, reason enough not to pull out patients’ teeth at the first visit." @default.
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• W2609105514 date "2017-04-26" @default.
• W2609105514 modified "2023-09-26" @default.
• W2609105514 title "Periodontitis and risk of psoriasis: another comorbidity" @default.
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• W2609105514 doi "https://doi.org/10.1111/jdv.14249" @default.
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